RESUMEN
Perfluorobutane sulfonate is a short-chain PFAS that is a less toxic replacement for the rather more toxic long-chain perfluorooctane sulfonate. PFBS is widespread in the environment and has raised environmental and health concerns. The study goal was to investigate whether dietary ingestion of PFBS would induce hepatic damage. Sprague-Dawley rats were assigned to three PFBS treatment groups for 11 weeks followed by clinical markers analyses in the serum and liver. There was a significant increase in liver and body weights of PFBS rats. Total antioxidant capacity was significantly reduced in the PFBS-treated group. ALT levels increased based on concentration ingested. Close to 1000 gene transcripts were differentially expressed. Further, transmembrane transport and oxidation-reduction processes were the most up-regulated biological processes. Inflammatory genes were up-regulated in the exposed group and those associated with oxidative damage were down-regulated. In conclusion, PFBS ingestion produced mild effects in the liver of Sprague Dawley rats.
Asunto(s)
Fluorocarburos , Hígado , Ratas Sprague-Dawley , Transcriptoma , Animales , Fluorocarburos/toxicidad , Hígado/metabolismo , Hígado/efectos de los fármacos , Masculino , Transcriptoma/efectos de los fármacos , Contaminantes Ambientales/toxicidad , Ratas , Ácidos Sulfónicos/toxicidad , Alanina Transaminasa/sangre , Peso Corporal/efectos de los fármacos , Dieta , Tamaño de los Órganos/efectos de los fármacosRESUMEN
Neurologic disease associated with migration of plant material is reported infrequently in dogs. Here we describe meningoencephalomyelitis associated with foreign plant material in a 2-y-old castrated male West Highland White Terrier dog with acute neck pain. Magnetic resonance imaging revealed spinal meningeal contrast enhancement. Although clinical signs improved after treatment with steroids, the dog was readmitted for further evaluation 3-mo later and was euthanized after generalized epileptic seizures. Autopsy findings consisted of coalescing, pus-filled, neuroparenchymal cavitations surrounded by hemorrhage in the left caudal colliculus and rostral left cerebellar hemisphere. Histologically, lesions consisted of necrosis and suppuration, which surrounded a 1 × 2-mm foreign body morphologically consistent with plant material and clusters of gram-positive bacterial cocci. Affected areas were surrounded by reactive astrocytes, fibrous connective tissue, and mixed inflammatory infiltrates. Areas of hemorrhage and infiltration by neutrophils and foamy macrophages with fibrinoid change of small capillaries were observed in the adjacent neuroparenchyma. The inflammation extended to the perivascular spaces in the leptomeninges (mesencephalon, cerebellum, and brainstem, and spinal cord) and spinal central canal. Anaerobic bacterial culture of frozen samples of cerebellum yielded heavy growth of Bacteroides pyogenes.
Asunto(s)
Enfermedades de los Perros , Meningoencefalitis , Perros , Animales , Meningoencefalitis/diagnóstico , Meningoencefalitis/veterinaria , Enfermedades de los Perros/diagnóstico , Médula Espinal/patología , Meninges/patología , Cerebelo/patologíaRESUMEN
Meningioangiomatosis (MA) is a rare proliferative meningovascular entity that has been described mainly in humans and dogs. Here we describe MA in a 13-y-old spayed female domestic shorthaired cat that died 5 d after acute change in behavior, open-mouth breathing, seizures, hyperthermia, and inability to walk. On MRI, the lesion appeared predominantly as extraparenchymal hemorrhage. Autopsy changes consisted of a dark-red, hemorrhagic plaque that expanded the leptomeninges and outer neuroparenchyma of the right piriform and temporal telencephalic lobes, chalky white nodules in the peripancreatic fat, and yellow fluid in the abdomen. Histologically, the lesion in the brain consisted of leptomeningeal thickening by spindle cells that effaced the subarachnoid spaces and extended perivascularly into the underlying cerebral cortex. Spindle cells were arranged as streams or whorls around blood vessels, and had slender eosinophilic cytoplasm and elongated nuclei with coarsely stippled chromatin and 1 or 2 distinct nucleoli. There was extensive hemorrhage, clusters of hemosiderin-laden macrophages, and mineralization throughout. Spindle cells had positive immunolabeling for vimentin. A striking MRI and gross feature in our case was the extensive hemorrhage associated with the MA lesion. Additional findings included suppurative pancreatitis with peritonitis and supraspinatus myonecrosis.